| First Author | Shim H | Year | 2012 |
| Journal | J Biol Chem | Volume | 287 |
| Issue | 18 | Pages | 14873-9 |
| PubMed ID | 22371490 | Mgi Jnum | J:184922 |
| Mgi Id | MGI:5426741 | Doi | 10.1074/jbc.M112.345751 |
| Citation | Shim H, et al. (2012) Defective retinal depolarizing bipolar cells in regulators of G protein signaling (RGS) 7 and 11 double null mice. J Biol Chem 287(18):14873-9 |
| abstractText | Two members of the R7 subfamily of regulators of G protein signaling, RGS7 and RGS11, are present at dendritic tips of retinal depolarizing bipolar cells (DBCs). Their involvement in the mGluR6/Galpha(o)/TRPM1 pathway that mediates DBC light responses has been implicated. However, previous genetic studies employed an RGS7 mutant mouse that is hypomorphic, and hence the exact role of RGS7 in DBCs remains unclear. We have made a true RGS7-null mouse line with exons 6-8 deleted. The RGS7(-/-) mouse is viable and fertile but smaller in body size. Electroretinogram (ERG) b-wave implicit time in young RGS7(-/-) mice is prolonged at eye opening, but the phenotype disappears at 2 months of age. Expression levels of RGS6 and RGS11 are unchanged in RGS7(-/-) retina, but the Gbeta5S level is significantly reduced. By characterizing a complete RGS7 and RGS11 double knock-out (711dKO) mouse line, we found that Gbeta5S expression in the retinal outer plexiform layer is eliminated, as is the ERG b-wave. Ultrastructural defects akin to those of Gbeta5(-/-) mice are evident in 711dKO mice. In retinas of mice lacking RGS6, RGS7, and RGS11, Gbeta5S is undetectable, whereas levels of the photoreceptor-specific Gbeta5L remain unchanged. Whereas RGS6 alone sustains a significant amount of Gbeta5S expression in retina, the DBC-related defects in Gbeta5(-/-) mice are caused solely by a combined loss of RGS7 and RGS11. Our data support the notion that the role of Gbeta5 in the retina, and likely in the entire nervous system, is mediated exclusively by R7 RGS proteins. |
